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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Dexamethasone and cardiac potassium currents in the diabetic rat.

Experiments were designed to compare effects of dexamethasone on transient (Ipeak) and sustained (Isus) K+ currents in control and diabetic rat myocytes. Ventricular myocytes were isolated from control or type 1 streptozotocin (STZ)-induced diabetic male and female rats. Currents were measured using whole-cell voltage-clamp methods. Incubation of cells from control males or females with 100 nM dexamethasone (5-9 h) significantly (P<0.005) augmented Isus (by 28-31%). Ipeak was unchanged. Isus augmentation was abolished by cycloheximide or cytochalasin D, but not by inhibition of protein kinases A or C. Inhibition of tyrosine kinases by genistein (but not its inactive analog genistin) prevented the increase of Isus by dexamethasone. In marked contrast, dexamethasone had a significantly (P<0.015) smaller effect on Isus (11% increase) in cells from male STZ-diabetic rats, as compared to control cells. However, Isus augmentation in cells from female STZ-diabetic rats was normal (31% increase). In ovariectomized-diabetic rats, Isus was unchanged by dexamethasone. The reduced effect in diabetic males might be due to preactivation of tyrosine kinases linking dexamethasone to current modulation. In conclusion, type I diabetes is associated with gender-specific changes in sensitivity of K+ currents to glucocorticoids, linked to alterations in tyrosine-phosphorylated proteins.[1]


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